SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Melander Olle) "

Sökning: WFRF:(Melander Olle)

  • Resultat 671-680 av 768
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
671.
  • Sun, Ryan, et al. (författare)
  • Integration of multiomic annotation data to prioritize and characterize inflammation and immune-related risk variants in squamous cell lung cancer
  • 2021
  • Ingår i: Genetic Epidemiology. - : John Wiley & Sons. - 0741-0395 .- 1098-2272. ; 45:1, s. 99-114
  • Tidskriftsartikel (refereegranskat)abstract
    • Clinical trial results have recently demonstrated that inhibiting inflammation by targeting the interleukin-1 beta pathway can offer a significant reduction in lung cancer incidence and mortality, highlighting a pressing and unmet need to understand the benefits of inflammation-focused lung cancer therapies at the genetic level. While numerous genome-wide association studies (GWAS) have explored the genetic etiology of lung cancer, there remains a large gap between the type of information that may be gleaned from an association study and the depth of understanding necessary to explain and drive translational findings. Thus, in this study we jointly model and integrate extensive multiomics data sources, utilizing a total of 40 genome-wide functional annotations that augment previously published results from the International Lung Cancer Consortium (ILCCO) GWAS, to prioritize and characterize single nucleotide polymorphisms (SNPs) that increase risk of squamous cell lung cancer through the inflammatory and immune responses. Our work bridges the gap between correlative analysis and translational follow-up research, refining GWAS association measures in an interpretable and systematic manner. In particular, reanalysis of the ILCCO data highlights the impact of highly associated SNPs from nuclear factor-kappa B signaling pathway genes as well as major histocompatibility complex mediated variation in immune responses. One consequence of prioritizing likely functional SNPs is the pruning of variants that might be selected for follow-up work by over an order of magnitude, from potentially tens of thousands to hundreds. The strategies we introduce provide informative and interpretable approaches for incorporating extensive genome-wide annotation data in analysis of genetic association studies.
  •  
672.
  • Surendran, Praveen, et al. (författare)
  • Trans-ancestry meta-analyses identify rare and common variants associated with blood pressure and hypertension
  • 2016
  • Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 48:10, s. 1151-1161
  • Tidskriftsartikel (refereegranskat)abstract
    • High blood pressure is a major risk factor for cardiovascular disease and premature death. However, there is limited knowledge on specific causal genes and pathways. To better understand the genetics of blood pressure, we genotyped 242,296 rare, low-frequency and common genetic variants in up to 192,763 individuals and used -1/4155,063 samples for independent replication. We identified 30 new blood pressure- or hypertension-associated genetic regions in the general population, including 3 rare missense variants in RBM47, COL21A1 and RRAS with larger effects (>1.5 mm Hg/allele) than common variants. Multiple rare nonsense and missense variant associations were found in A2ML1, and a low-frequency nonsense variant in ENPEP was identified. Our data extend the spectrum of allelic variation underlying blood pressure traits and hypertension, provide new insights into the pathophysiology of hypertension and indicate new targets for clinical intervention.
  •  
673.
  • Svensson, Akiko Kishi, et al. (författare)
  • Incident diabetes mellitus may explain the association between sleep duration and incident coronary heart disease
  • 2018
  • Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 0012-186X .- 1432-0428. ; 61:2, s. 331-341
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims/hypothesis: Sleep duration is a risk factor for incident diabetes mellitus and CHD. The primary aim of the present study was to investigate, in sex-specific analyses, the role of incident diabetes as the possible biological mechanism for the reported association between short/long sleep duration and incident CHD. Considering that diabetes is a major risk factor for CHD, we hypothesised that any association with sleep duration would not hold for cases of incident CHD occurring before incident diabetes (‘non-diabetes CHD’) but would hold true for cases of incident CHD following incident diabetes (‘diabetes-CHD’). Methods: A total of 6966 men and 9378 women aged 45–73 years from the Malmö Diet Cancer Study, a population-based, prospective cohort, who had answered questions on habitual sleep duration and did not have a history of prevalent diabetes or CHD were included in the analyses. Incident cases of diabetes and CHD were identified using national registers. Sex-specific Cox proportional hazards regression models were stratified by BMI and adjusted for known covariates of diabetes and CHD. Results: Mean follow-up times for incident diabetes (n = 1137/1016 [men/women]), incident CHD (n = 1170/578), non-diabetes CHD (n = 1016/501) and diabetes-CHD (n = 154/77) were 14.2–15.2 years for men, and 15.8–16.5 years for women. In men, short sleep duration (< 6 h) was associated with incident diabetes (HR 1.35, 95% CI 1.01, 1.80), CHD (HR 1.41, 95% CI 1.06, 1.89) and diabetes-CHD (HR 2.34, 95% CI 1.20, 4.55). Short sleep duration was not associated with incident non-diabetes CHD (HR 1.35, 95% CI 0.98, 1.87). Long sleep duration (≥ 9 h) was associated with incident diabetes (HR 1.37, 95% CI 1.03, 1.83), CHD (HR 1.33, 95% CI 1.01, 1.75) and diabetes-CHD (HR 2.10, 95% CI 1.11, 4.00). Long sleep duration was not associated with incident non-diabetes CHD (HR 1.33, 95% CI 0.98, 1.80). In women, short sleep duration was associated with incident diabetes (HR 1.53, 95% CI 1.16, 2.01), CHD (HR 1.46, 95% CI 1.03, 2.07) and diabetes-CHD (HR 2.88, 95% CI 1.37, 6.08). Short sleep duration was not associated with incident non-diabetes CHD (HR 1.29, 95% CI 0.86, 1.93). Conclusions/interpretation: The associations between sleep duration and incident CHD directly reflect the associations between sleep duration and incident diabetes. Incident diabetes may thus be the explanatory mechanism for the association between short and long sleep duration and incident CHD.
  •  
674.
  • Svensson, Patrik, et al. (författare)
  • A functional variant of the NEDD4L gene is associated with beneficial treatment response with β-blockers and diuretics in hypertensive patients.
  • 2011
  • Ingår i: Journal of Hypertension. - 1473-5598. ; 29:2, s. 388-395
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: The capability of the protein NEDD4L to reduce renal tubular expression of epithelial Na+ channel (ENaC) is influenced by a functional rs4149601 G→A NEDD4L polymorphism. As diuretics and β-blockers inhibit renal sodium reabsorption and renin release, respectively, we hypothesized that the β-blocker or diuretic-induced blood pressure reduction and prevention of cardiovascular disease would be greater in patients with the highest ENaC expression (rs4149601 G-allele), whereas there would be no such genetically mediated differences in treatment efficacy among patients treated with the vasodilator diltiazem. METHODS: We related rs4149601 status to 6-month blood pressure reduction and risk of cardiovascular events in 5152 hypertensive patients (DBP ≥ 100 mmHg) from the Nordic Diltiazem Study (NORDIL) randomized to either β-blocker and/or diuretic-based treatment or diltiazem-based treatment. RESULTS: In patients on β-blocker or diuretic monotherapy, carriers of the G-allele had greater SBP reduction (19.5 ± 16.8 vs. 15.0 ± 19.3 mmHg, P < 0.001) and DBP reduction (15.4 ± 8.3vs. 14.1 ± 8.4 mmHg, P = 0.02) and during 4.5 years of follow-up among patients randomized to β-blockers and/or diuretics, carriers of the G-allele had greater protection from cardiovascular events [relative risk (RR) = 0.52, 95% confidence interval (CI) = 0.36-0.74, P < 0.001] as compared to AA homozygotes. Within the diltiazem group, there was no difference in blood pressure reduction or risk of cardiovascular events according to genotype. CONCLUSION: The functional NEDD4L rs4149601 polymorphism influences the efficacy of β-blocker and/or diuretic-based antihypertensive treatment both in terms of blood pressure reduction and cardiovascular disease protection, whereas diltiazem-based antihypertensive treatment efficacy is not influenced by this NEDD4L polymorphism.
  •  
675.
  •  
676.
  • Svensson, Patrik, et al. (författare)
  • Cystatin C Is Not Causally Related to Coronary Artery Disease.
  • 2015
  • Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 10:6
  • Tidskriftsartikel (refereegranskat)abstract
    • Strong and independent associations between plasma concentration of cystatin C and risk of cardiovascular disease (CVD) suggests causal involvement of cystatin C.
  •  
677.
  •  
678.
  • Svensson, Patrik, et al. (författare)
  • Interaction Between Renal Function and Microalbuminuria for Cardiovascular Risk in Hypertension The Nordic Diltiazem Study
  • 2008
  • Ingår i: Hypertension. - 1524-4563. ; 52:1, s. 115-122
  • Tidskriftsartikel (refereegranskat)abstract
    • We investigated whether renal function and microalbuminuria are independent predictors and whether any interaction exists between them, regarding future cardiovascular disease in hypertensive patients (n=10 881) followed for 4.5 years. The primary end points (PEs) were fatal and nonfatal myocardial infarction and stroke and other cardiovascular deaths. Creatinine and glomerular filtration rate (GFR), estimated using the formulas of the Modification of Diet in Renal Disease study group and Cockroft and Gault and in a subsample (n=4929) of microalbuminuria and interaction terms of microalbuminuria and renal function, were related to the risk of the PE using Cox proportional hazards model after full adjustment. Increased creatinine (P < 0.001), decreased GFR from Cockroft and Gault (P=0.001), and decreased GFR from the Modification of Diet in Renal Disease study group (P=0.001) were all independent risk factors for the PE. Stepwise exclusion of patients with the poorest renal function excluded the possibility that the relationship between decreasing renal function and the PE was driven only by patients with severely impaired renal function. Microalbuminuria and all 3 of the indices of renal function predicted the PE independent of each other. There was a significant interaction between microalbuminuria and GFR from Cockroft and Gault (P=0.040) in prediction of the PE. Both renal function and microalbuminuria add independent prognostic information regarding cardiovascular risk in hypertensive patients. The cardiovascular risk associated with microalbuminuria increases with a decline in GFR, as demonstrated by a significant interaction between microalbuminuria and GFR from Cockroft and Gault. Because estimation of the total cardiovascular risk is essential for the aggressiveness of risk factor interventions, simultaneous inclusion of GFR and microalbuminuria in global cardiovascular risk assessment is essential. (Hypertension. 2008;52:115-122.)
  •  
679.
  • Svensson, Thomas, et al. (författare)
  • A genetic risk score for CAD, psychological stress, and their interaction as predictors of CAD, fatal MI, non-fatal MI and cardiovascular death
  • 2017
  • Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 12:4
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Psychological stress is an independent risk factor for cardiovascular disease (CVD), but the mechanism by which stress is associated with CVD is not entirely understood. Although genetic factors are implied in both stress responsivity and cardiovascular reactivity, no studies to date have investigated their interactions with stress for cardiovascular end points. The objective was to elucidate the association and interactions between a genetic risk score (GRS), individual genetic variants and stress for three cardiovascular end points: Coronary artery disease (CAD), fatal myocardial infarction (MI), non-fatal MI, and cardiovascular death. Methods and findings 18,559 participants from the Malmö Diet Cancer Study, a population-based prospective study, were included in the analyses. Cox proportional hazards regression models were used and adjusted for a large number of known predictors of cardiovascular end points. Mean follow-up time in years was 14.6 (CAD; n = 1938), 14.8 (fatal MI; n = 436), 14.8 (nonfatal MI; n = 1108), and 15.1 (cardiovascular death; n = 1071) respectively. GRS was significantly associated with increased risks of CAD (top quartile hazard ratio [HR], 1.72; 95% confidence interval [CI], 1.51±1.96), fatal MI (top quartile HR, 1.62; 95%CI, 1.23-2.15), nonfatal MI (top quartile HR, 1.55; 95%CI, 1.31±1.84), and cardiovascular death (top quartile HR, 1.29; 95%CI, 1.08-1.53). Stress was not independently associated with any end point and did not interact with GRS. Four individual genetic variants interacted unfavorably with stress for end points with mortality outcomes. Conclusion A GRS composed of 50 SNPs and predictive of CAD was found for the first time to also strongly predict fatal MI, non-fatal MI and cardiovascular death. A stress-sensitive component of the GRS was isolated on the basis of individual genetic variants that interacted unfavorably with stress.
  •  
680.
  • Svensson, Thomas, et al. (författare)
  • Psychological stress and risk of incident atrial fibrillation in men and women with known atrial fibrillation genetic risk scores
  • 2017
  • Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 7
  • Tidskriftsartikel (refereegranskat)abstract
    • Psychological stress has been reported as a possible trigger of atrial fibrillation (AF). No studies have investigated whether any association between stress and AF could be modified by genetic susceptibility to AF (AF-genetic risk score (AF-GRS)). 8765 men and 13,543 women from the Malmö Diet Cancer Study, a population-based cohort, were included in the analyses. A variable representing stress was constructed from questions measuring job strain, and from one question assessing non-occupational stress. Cox proportional hazards regression models were adjusted for known covariates of AF. Mean follow-up times and number of recorded incident AF were 14.2 years and 1116 events for men, and 15.1 years and 932 events for women. Among women, high stress was associated with AF in the age adjusted model (hazard ratio [HR], 1.22; 95% confidence interval [CI], 1.01-1.47) but not following multivariable adjustment (HR, 1.15; 95% CI, 0.95-1.39). Stress was not associated with incident AF in men. AF-GRS was significantly associated with incident AF for both genders. Stress did not interact significantly with genetic susceptibility to AF in men or women. Chronic stress is not associated with long-term incident hospital diagnosed AF. This association does not appear to be modified by genetic susceptibility to AF.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 671-680 av 768
Typ av publikation
tidskriftsartikel (719)
konferensbidrag (29)
rapport (7)
forskningsöversikt (6)
doktorsavhandling (3)
bokkapitel (3)
visa fler...
samlingsverk (redaktörskap) (1)
visa färre...
Typ av innehåll
refereegranskat (738)
övrigt vetenskapligt/konstnärligt (30)
Författare/redaktör
Melander, Olle (760)
Engström, Gunnar (191)
Orho-Melander, Marju (146)
Hedblad, Bo (113)
Almgren, Peter (105)
Nilsson, Peter (75)
visa fler...
Groop, Leif (73)
Nilsson, Peter M (73)
Fedorowski, Artur (64)
Kathiresan, Sekar (51)
Persson, Margaretha (44)
Fava, Cristiano (44)
Sjögren, Marketa (41)
Nilsson, Jan (41)
Magnusson, Martin (40)
Smith, Gustav (40)
Lind, Lars (38)
Salomaa, Veikko (37)
Samani, Nilesh J. (37)
Borné, Yan (35)
Berglund, Göran (35)
Boerwinkle, Eric (33)
Sutton, Richard (33)
Newton-Cheh, Christo ... (31)
Wareham, Nicholas J. (30)
Enhörning, Sofia (29)
Hamrefors, Viktor (28)
Danesh, John (28)
Overvad, Kim (26)
O'Donnell, Christoph ... (26)
Ottosson, Filip (26)
Struck, Joachim (25)
Hindy, George (25)
Loos, Ruth J F (25)
Bergmann, Andreas (25)
Tumino, Rosario (24)
Padmanabhan, Sandosh (24)
Deloukas, Panos (23)
Chasman, Daniel I. (23)
Langenberg, Claudia (23)
Fernandez, Celine (23)
van der Schouw, Yvon ... (23)
Voight, Benjamin F. (23)
Boeing, Heiner (22)
Tuomi, Tiinamaija (22)
Franks, Paul W. (22)
Ricci, Fabrizio (22)
Psaty, Bruce M (22)
Gudnason, Vilmundur (22)
Wang, Thomas J (22)
visa färre...
Lärosäte
Lunds universitet (711)
Umeå universitet (63)
Uppsala universitet (59)
Karolinska Institutet (50)
Göteborgs universitet (46)
Linköpings universitet (15)
visa fler...
Malmö universitet (8)
Naturvårdsverket (7)
Högskolan Kristianstad (5)
Stockholms universitet (5)
Chalmers tekniska högskola (3)
Högskolan Dalarna (3)
Linnéuniversitetet (2)
Kungliga Tekniska Högskolan (1)
Luleå tekniska universitet (1)
Högskolan i Halmstad (1)
Örebro universitet (1)
Högskolan i Skövde (1)
Sveriges Lantbruksuniversitet (1)
visa färre...
Språk
Engelska (753)
Svenska (15)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (744)
Naturvetenskap (28)
Samhällsvetenskap (2)
Humaniora (2)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy